Identification of human hornerin and its expression in regenerating and psoriatic skin.

TL;DR: It is concluded that IL‐17A downregulates the expression of filaggrin and genes important for cellular adhesion which could affect epidermal barrier formation.

TL;DR: The results show that the changes accompanying the transition from non-lesional to acute to chronic inflammation in AD are quantitative rather than qualitative, with chronic AD having heightened Th2, Th1, Th17, and IL36 responses and skin barrier repair mechanisms.

TL;DR: In this overview, the complete life of keratinocytes is described, from the proliferative organization to the process of desquamation.

TL;DR: Immunoelectron microscopy demonstrated that PAD1 and PAD3 are co-located with filaggrin within the filamentous matrix of the deeper corneocytes where the protein is deiminated, which strongly suggests that both isoforms are involved in the deimination of filag Grin.

TL;DR: It is concluded that the re-formation of microtubules and reassembly of a nuclear transport-competent envelope do not depend on chromosome decondensation.

TL;DR: Hornerin was expressed in the upper epidermis of newborn mouse skin, as was profilaggrin, and both genes were expressed at highest levels in the forestomach and at the nexthighest levels in skin, which form the basis for a better understanding of possible overlapping and/or differential functions of hornerin and profilggrin.

TL;DR: By use of PCR analyses, it is found that human loricrin consists of two allelic size variants, due to sequence variations in the second glycine loop domain only, and these variants segregate in the human population by normal Mendelian mechanisms.